AB0248 LIPID PROFILE CHANGES FROM PRE-CLINICAL TO ESTABLISHED RHEUMATOID ARTHRITIS: A 12 YEARS FOLLOWUP PILOT STUDY
Authors: R. Raadsen, L. Van Boheemen, M. Nurmohamed
Journal: Annals of the Rheumatic Diseases (2022)

Background Patients with rheumatoid arthritis (RA) have an increased risk for developing cardiovascular diseases (CVD). This is partly due to the systemic inflammation characteristic to the disease, but also due to an increased prevalence of ‘traditional’ risk factors such as dyslipidemia. The inflammation in RA often leads to an increased catabolism of lipids, resulting in a subsequent decrease in HDL and LDL, while treatment with anti-inflammatory medication reverses these effects. This decreased cholesterol level in active disease is, unexpectedly, associated with an increased incidence of CVD (the lipid paradox). Additionally, we previously demonstrated pro-atherogenic lipid profile changes in preclinical RA patients. Objectives To explore the lipid profile changes in RA patients through different phases of the disease, i.e. from the preclinical stage and RA onset through treatment with biological disease modifying anti-rheumatic drugs (bDMARDs). Methods Thirty-nine consecutive patients who were previously included in both Reade’s RA prevention cohort and biological cohort were included in the current study. The prevention cohort consisted of individuals with arthralgia and rheumatoid factor and/or anti-citrullinated protein antibodies without arthritis, and the biological cohort comprised RA patients using bDMARDs. Lipid spectrum was measured longitudinally, at the following points in the disease course identified in each patient (time from baseline was different in each patient due to the natural course of disease progression): 1.Baseline, months prior to RA diagnosis (Start Prevention cohort) 2.Moment of RA diagnosis (End Prevention cohort) 3.Period between diagnosis and start bDMARD treatment 4.Start treatment with bDMARDs 5-7.Continued treatment with bDMARDs Results From baseline, high density lipoprotein cholesterol (HDLc) and apolipoprotein A1 (ApoA1) increased up to the start of biological treatment, thereafter they slightly decreased. Low density lipoprotein cholesterol (LDLc) and apolipoprotein B (ApoB) both decreased with higher disease activity, increasing again after starting bDMARD therapy. Total cholesterol/HDL ratio decreased substantially from baseline and onwards and stabilized in the bDMARDs treatment phase. Lipoprotein(a) (Lp(a)) increased slightly up to treatment with bDMARDs, after which it stabilized. Figure 1 shows the progression of HDLc, LDLc and total cholesterol (TC) plotted against C-reactive protein (CRP) over time. Figure 1. Time course of cholesterol parameters vs disease activity. CRP = C-reactive protein, RA = rheumatoid arthritis, Dx = diagnosis, TC = total cholesterol, HDL = high-density lipoprotein, LDL = low-density lipoprotein Conclusion Our study uniquely shows the change of lipid parameters during the course of RA disease. While LDLc, ApoB and cholesterol/HDL ratio decreased with higher disease activity, HDLc and ApoA1 increased, affirming the expectations. Larger cohort studies are necessary to accurately elucidate the development of lipids through different disease stages in RA patients, to better understand one of the key risk factors for CVD in RA. References [1]van Halm, V. P. et al. (2007). Lipids and inflammation: serial measurements of the lipid profile of blood donors who later developed rheumatoid arthritis. Annals of the rheumatic diseases , 66 (2), 184–188. Disclosure of Interests None declared